Glucagon-like peptides 1 and 2 in health and disease: A review

Marathe, Chinmay S.; Rayner, Christopher K.; Jones, Karen L.

doi:10.1016/j.peptides.2013.01.014

Cited by 78 publications

(67 citation statements)

References 152 publications

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“…The anorexigenic GLP-1 and PYY hormones were significantly higher in both fasting and postprandial conditions. GLP-1, a member of a subfamily that includes secretin, gastric inhibitory peptide (GIP) and VIP, is produced by intestinal L cells following food ingestion to stimulate glucose-dependent insulin secretion, β-cell growth and survival, as well as to inhibit glucagon release, gastric emptying and food intake (Marathe, 2013). For these hormonal effects, the GLP-1 system has been targeted (Garber, 2011) by using GLP-1 receptor agonists and dipeptidyl peptidase-4 (DPP-4) inhibitors of GLP-1 degradation in order to establish new therapeutic approaches for treating type 2 diabetes and to promote satiety and body weight loss.…”

Section: Discussionmentioning

confidence: 99%

Regulation of Appetite, Body Composition, and Metabolic Hormones by Vasoactive Intestinal Polypeptide (VIP)

Larauche

Flores

et al. 2015

J Mol Neurosci

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Introduction Vasoactive Intestinal Peptide (VIP) is a 28-amino acid neuropeptide that belongs to the secretin-glucagon superfamily of peptides and has 68% homology with PACAP. VIP is abundantly expressed in the central and peripheral nervous system and in the gastrointestinal tract, where it exercises several physiological functions. Previously, it has been reported that VIP regulates feeding behavior centrally in different species of vertebrates such as goldfishes, chicken, and rodents. Additional studies are necessary to analyze the role of endogenous VIP on the regulation of appetite/satiety together with feeding behavior, metabolic hormone release, body mass composition and energy balance. Aims To elucidate the physiological pathways by which VIP regulates appetite/satiety, feeding behavior, metabolic hormones and body mass composition. Methods VIP deficient (VIP −/−) and age-matched wild-type (WT) littermates were weekly monitored from 5 to 22 weeks of age using a whole body composition EchoMRI analyzer. Food intake and feeding behavior were analyzed using the BioDAQ automated monitoring system. Plasma levels of metabolic hormones including active-ghrelin, GLP-1, leptin, PYY, pancreatic polypeptide (PP), adiponectin, and insulin were measured in fasting as well as in postprandial conditions. Results The genetic lack of VIP led to a significant reduction of body weight and fat mass and to an increase of lean mass as the mice aged. Additionally, VIP−/− mice had a disrupted pattern of circadian feeding behavior resulting in an abolished regular nocturnal/diurnal feeding. These changes were associated with an altered secretion of adiponectin, GLP-1, leptin, PYY and insulin in VIP−/− mice. Our data demonstrates that endogenous VIP is involved in the control of appetite/satiety, feeding behavior, body mass composition and in the secretion of six different key regulatory metabolic hormones. Conclusions Our data show that endogenous VIP is involved in the control of appetite/satiety, feeding behavior, body mass composition and in the secretion of six key regulatory metabolic hormones. VIP plays a key role in the regulation of body weight and mass composition phenotype by significantly enhancing body weight and fat mass accumulation. Therefore, VIP signaling is critical for the modulation of appetite/satiety and body mass phenotype and is suggested to be a target for future treatment of obesity.

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Section: Discussionmentioning

confidence: 99%

Regulation of Appetite, Body Composition, and Metabolic Hormones by Vasoactive Intestinal Polypeptide (VIP)

Larauche

Flores

et al. 2015

J Mol Neurosci

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“…GLP-1 is intimately involved in the regulation of circulating blood glucose, acting to increase insulin secretion and sensitivity in a glucosedependent manner. It is well established that GLP-1 has many effects on multiple organ systems related to nutrient ingestion and blood glucose homeostasis [6,7]. In the gastrointestinal system, GLP-1 inhibits gastrointestinal motility, reduces gastric acid secretion, and slows gastric emptying [8][9][10][11].…”

Section: Glp-1: An Overviewmentioning

confidence: 99%

“…GLP-1 has been shown to suppress appetite in both normal and obese individuals, thereby reducing food intake [12][13][14][15]. In the pancreas, GLP-1 stimulates insulin secretion from β-cells in a blood-glucose dependent manner, while also inhibiting glucagon secretion in α-cells, thus playing an essential role in blood glucose regulation [6,7].…”

Section: Glp-1: An Overviewmentioning

confidence: 99%

“…This review focuses on recent discoveries on GLP-1 production in pancreatic islets and its action within pancreatic tissue. There are a number of outstanding and comprehensive reviews regarding general GLP-1 biology, physiology, and its therapeutic use, but few focusing specifically on GLP-1 production in pancreas as well as its function and regulation within the pancreas [7,[21][22][23][24]. …”

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confidence: 99%

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Pancreatic Glucagon-Like Peptide 1: What is known?

Fava¹,

2014

J Diabetes Metab 2013

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Glucagon-like peptide-1 (GLP-1) is an incretin hormone encoded together with glucagon by the proglucagon gene. It has been widely accepted that GLP-1 and glucagon are derived from distinct post-translational processing of proglucagon in a tissue specific manner. GLP-1 is produced in intestinal L-cells where proglucagon is processed by prohormone convertase 1/3 (PC1/3), while glucagon is produced in pancreatic α-cells via PC2-mediated cleavage. Nonetheless, emerging evidence has now demonstrated GLP-1 is also produced in pancreatic islets, although its concentration is much lower than glucagon. Further studies have shown GLP-1 production and secretion can be up-regulated by various factors, in particular, hyperglycemia and β-cell damage. The importance of locally produced GLP-1 in pancreas for β-cell function has started to be recognized. Similar to circulating GLP-1, α-cell produced GLP-1 can promote insulin secretion, protect β-cells and enhance β-cell proliferation, thus is vital for β-cell function. This review focuses on these recent discoveries regarding GLP-1 production in pancreatic islets and its action within pancreatic tissue.Keywords: GLP-1; Alpha cells; Islets; Diabetes; PC1/3 GLP-1: An OverviewGlucagon-like peptide-1 (GLP-1) is one of the peptide hormones encoded by the proglucagon gene, which gives rise to a number of individual peptides through posttranslational processing [1][2][3][4][5]. Based on its origin within the intestine and its vital role in stimulating insulin secretion, GLP-1 is considered a member of the incretin family. GLP-1 is intimately involved in the regulation of circulating blood glucose, acting to increase insulin secretion and sensitivity in a glucosedependent manner. It is well established that GLP-1 has many effects on multiple organ systems related to nutrient ingestion and blood glucose homeostasis [6,7]. In the gastrointestinal system, GLP-1 inhibits gastrointestinal motility, reduces gastric acid secretion, and slows gastric emptying [8][9][10][11]. GLP-1 has been shown to suppress appetite in both normal and obese individuals, thereby reducing food intake [12][13][14][15]. In the pancreas, GLP-1 stimulates insulin secretion from β-cells in a blood-glucose dependent manner, while also inhibiting glucagon secretion in α-cells, thus playing an essential role in blood glucose regulation [6,7].GLP-1 and glucagon share ~50% homology, deriving from the same precursor-proglucagon. The diversification takes place at the posttranslational stage in a tissue-specific manner (Figure 1). In pancreatic α-cells, proglucagon is mainly cleaved by prohormone Convertase 2 (PC2), giving rise to glucagon, Intervening Peptide-1 (IP-1), GlicentinRelated Polypeptide (GRPP), and the Major Proglucagon Fragment (MPGF) [16][17][18]. In contrast, in enteroendocrine L-cells, proglucagon is processed by prohormone convertase 1/3 (PC1/3), resulting in the production of GLP-1, GLP-2, glicentin, and several other small peptides [19,20].Nonetheless, emerging evidence has now demonstrated that GL...

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“…Incretin hormones are components of the intestinal-pancreatic axis and play an important role in postprandial increase in insulin secretion by b-cells of the pancreas. These hormones are responsible for the so-called 'incretin effect', which consist in a significantly stronger insulin response to oral intake of glucose-containing food than to the same amount of glucose administered intravenously [1,2]. Meal ingestion stimulates L-cells of the mucous membrane of the small intestine to synthesise and secrete incretin hormones that reach the pancreatic b-cells through the blood vessels and stimulate insulin secretion even before the glucose concentration in the intercellular fluid of the pancreatic is increased [3].…”

Section: Introductionmentioning

confidence: 99%